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Overview of Facial Paralysis


Thomas Schubert

, DVM, DACVIM, DABVP, Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida

Last full review/revision Jun 2013 | Content last modified Jun 2013

Asymmetry of facial expression is common with unilateral lesions of the facial nucleus or nerve in most species. Bilateral facial paralysis may be more difficult to recognize, but affected animals drool and have a dull facial expression. Complete facial paralysis is an inability to move the eyelids, ears, lips, or nostrils. Facial paresis is reduced movement of the muscles of facial expression and indicates milder nucleus or nerve involvement. The nucleus of the facial nerve is located in the rostral medulla oblongata of the brain stem. The facial nerve, cranial nerve VII, exits the brain stem near the vestibulocochlear nerve, passes through the petrous temporal bone, and then exits the skull through the stylomastoid foramen and splits into auricular, palpebral, and buccal branches.

Clinical Findings and Lesions:

Clinical signs of facial paralysis vary with the location, severity, and chronicity of the lesion. If a unilateral lesion is located in the facial nucleus or proximal portion of the facial nerve, paresis or paralysis of the eyelids, ears, lips, and nostrils on that side are seen. A lesion of the auriculopalpebral branch of the facial nerve, near the zygomatic arch, results in paresis or paralysis of the eyelids and ear only. A lesion of the palpebral branch of the facial nerve, crossing the zygomatic arch, results in paresis or paralysis of the eyelids only. A lesion of the buccal branch of the facial nerve, as it courses along the surface of the masseter muscles, results in paresis or paralysis of the lips and nostrils only.

In small animals with facial paralysis, the palpebral fissure may be slightly larger on the affected side; in horses and food animals, the palpebral fissure is slightly smaller because of a loss of tone in the frontalis muscles above the eyelid. When the medial or lateral canthus of the eyelids or cornea are touched, the eyelids do not close, but the eyeball will retract into the orbit (if the trigeminal and abducent nerves are functioning properly). The third eyelid will passively elevate as the globe retracts. If both eyes are tested simultaneously, movement on each side can be compared. When the animal is unable to blink the eye, corneal irritation may result in excessive tear production. In acute denervation, the ear carriage is often lower on the side of the lesion in all species, but in chronic denervation with muscle fibrosis and contracture, the ear carriage may be higher. The fibrosis of the auricular muscles can be palpated, and the ear becomes adhered in the abnormal position. In acute lesions, the lips on the paralyzed side may hang loosely, exposing mucosa. When the animal eats or drinks, food and fluids may fall from the lips. The animal may drool excessively, and food may collect between the lips and teeth. In chronic lesions, fibrosis of the lip muscles can be palpated, and the lip on the affected side is higher than on the normal side. In acute, unilateral lesions, the nose deviates away from the side of the lesion, owing to a loss in muscle tone on the affected side. In horses, the affected nostril is unable to dilate on inspiration. In chronic lesions, muscle fibrosis and contracture cause the nose to deviate toward the lesion, and the muscles feel firm and inflexible. Because the facial nerve provides sensory innervation to the distal tongue, a bitter substance such as atropine will not be recognized when placed on the distal tongue.

Often, the parasympathetic portion of the facial nerve is also affected, and tear and saliva production on the side of the lesion is reduced or absent. Reduced or absent tear production, with eyelid paresis or paralysis, can result in corneal exposure with resultant ulceration. In cases of facial nerve paralysis, a Schirmer tear test can be used to determine whether administration of artificial tears is needed. Reduced saliva production can result in dry mucous membranes, and food may collect in the buccal folds. Dryness on the side of the lesion can be detected by simultaneously palpating the mucous membranes on both sides and comparing the degree of moisture.

Other concomitant neurologic deficits can further localize the facial nerve lesion. If the animal has ataxia, hemiparesis, quadriparesis, or conscious proprioceptive deficits associated with facial nerve paralysis, a brain-stem lesion is probable. If the animal has facial paralysis with a head tilt, nystagmus, or other evidence of vestibular deficits, but no hemiparesis, quadriparesis, or conscious proprioceptive deficits, then a lesion of the facial nerve exists as it exits the brain stem or passes through the petrous temporal bone. If a small animal has facial paralysis with ptosis, miosis, and enophthalmos (Horner syndrome), a lesion of the middle ear is likely.

Diagnosis and Treatment:

Trauma is a common cause of facial paralysis in all species. In horses, halter injuries and prolonged lateral recumbency may injure the buccal branches of the facial nerve on the side of the jaw and cause unilateral or bilateral paresis or paralysis of the lips and nostrils. Cattle that struggle in stanchions may injure the palpebral branch of the facial nerve as it crosses the zygomatic arch, causing unilateral or bilateral paresis or paralysis of the eyelid(s). Small animals may incur peripheral facial nerve injuries from rough handling, automobile accidents, or surgery such as bulla osteotomy and total ear ablation. Electromyography, including electrical stimulation of the facial nerve, can be used to determine the location and severity of the injury; however, changes will not be evident until 5–7 days after injury.

Therapy for injury may include massage and heat of denervated muscles for 15 min, 2−3 times/day, to maintain their integrity while awaiting any nerve regeneration. Laser therapy, also known as cold laser, low level light therapy, or photobiomodulation, can help nerve regeneration. The facial nerve can regenerate ~1–4 mm/day, so serial neurologic examinations can also help determine the prognosis. If there has been no improvement after 6 mo, the chance of recovery is poor. Horses with collapsing nostrils may require corrective surgery. Species that need the lips for drinking and prehending food must be given deep water containers and wet bulky mashes.

Otitis media is another common cause of facial paralysis in all species, especially in dogs with chronic dermatitis. Otitis externa and a ruptured or diseased tympanic membrane are often seen on otoscopic examination under general anesthesia. Despite an intact tympanum, 16% of animals with acute otitis externa may have otitis media, and as many as 89% of animals with chronic otitis externa may have otitis media (also see Otitis Externa and {blank} Otitis Media and Interna). Skull radiographs, CT, and MRI may be necessary to confirm otitis media. The prognosis can be good if the diagnosis is made early and the animal is treated for 4–6 wk with the appropriate antibiotic, determined by culture and sensitivity on a sample obtained via myringotomy. Corticosteroids should be avoided because they may encourage osteomyelitis. The facial nerve paralysis can be permanent, and longterm administration of artificial tears may be necessary.

Guttural pouch infections (see Guttural Pouch Disease in Horses) can produce facial paralysis in horses. Lesions of the facial nerve nucleus can result in facial nerve paralysis in equine protozoal myeloencephalitis (EPM, see Equine Protozoal Myeloencephalitis). CSF analysis and titers for EPM are essential for diagnosis and institution of appropriate therapy.

Idiopathic facial nerve paralysis is common in dogs and is diagnosed by excluding other diseases. Otitis media must be excluded with examination and radiographs. Because hypothyroidism (see Hypothyroidism in Animals) can cause facial nerve paralysis, levels of thyroxine (T4) and thyroid-stimulating hormone should be determined in all dogs with facial paralysis. Thyroid replacement therapy may not always resolve facial paralysis in hypothyroid dogs. If there is no infection, thyroid function is normal, and there has been no known trauma, the diagnosis of idiopathic facial paralysis is made. There is no therapy. Artificial tear administration may be necessary. Facial paralysis can be unilateral or bilateral and can resolve spontaneously or be permanent. It can occur on one side, resolve, and then occur on the other side at a later time. Permanent paralysis may be disfiguring but does not affect the quality of life in dogs.

Primary neoplasia of the facial nerve is rare, but dogs and cats can develop a neoplastic process that affects middle ear structures, including the facial nerve. Squamous cell carcinoma and polyps of the middle ear are most common in cats. Otoscopy of the external ear canal under anesthesia with biopsy and histologic examination of abnormal tissue can assist with the diagnosis. CT and MRI of the osseous bulla are necessary to determine the extent of the lesion before surgery. Early radical excision of the tumor and radiation, if indicated, may afford a good longterm prognosis depending on tumor type.

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